1. Technical Field
This document relates to methods and materials for treating diseases or disorders associated with elevated platelet counts (e.g., essential thrombocythemia, secondary thrombocytosis, congenital amegakaryocytic thrombocytopenia, sepsis, or asplenism). This document also relates to methods and materials for treating diseases or disorders associated with elevated platelet adhesion to collagen (e.g., acute coronary syndromes, angina pectoris, chronic atherosclerosis, diabetes, or hypertension).
2. Background Information
The family of natriuretic peptides (NPs) contains three members: atrial natriuretic peptide (ANP), b-type natriuretic peptide (BNP), and c-type natriuretic peptide (CNP). Each of these are cardiovascular-protective in nature and participate in regulatory roles in health and disease. While ANP and BNP are of cardiac origin, CNP is primarily derived from the endothelium as well as bone and brain. The biological actions of NPs are mediated through membrane-bound natriuretic peptide receptors (NPRs). NPR-A (or GC-A) and NPR-B (or GC-B) are guanylyl cyclase linked and activate the cyclic guanosine monophosphate-(cGMP) dependent signaling cascade. ANP and BNP activate GC-A to generate 3′, 5′ cyclic guanosine monophosphate (cGMP), while CNP activates cGMP through the GC-B receptor.